Top

Published in:

01-09-2013 | Nutrition and Lifestyle in Osteoporosis (S Ferrari, Section Editor)

Influence of Hormonal Appetite and Energy Regulators on Bone

Authors: Ee Cheng Khor, Natalie Kah Yun Wee, Paul A Baldock

Published in: Current Osteoporosis Reports | Issue 3/2013

Abstract

Nutritional status is an essential component in determining whole body energy homeostasis. The balance between energy/food intake and metabolism is governed by a range of hormones secreted from various parts of the body. Their subsequent dissemination via the blood results in a wide range of biological responses including satiety, hunger, and glucose uptake. The roles of these systemic hormones also extend to bone regulation with animal and clinical studies establishing a relationship between these regulatory pathways. This review covers the gastrointestinal hormones, ghrelin, PYY, GIP, GLP-1, and GLP-2, and the adipokines, leptin, and adiponectin and their roles in regulating bone homeostasis. Their known actions are reviewed, with an emphasis upon recent advances in understanding. Taken together, this review outlines an expanding appreciation of the interactions between bone mass and the nutritional control of whole body energy balance by gut and adipose tissue.

Clowes JA, Hannon RA, Yap TS, Hoyle NR, Blumsohn A, Eastell R. Effect of feeding on bone turnover markers and its impact on biological variability of measurements. Bone. 2002;30(6):886–90.PubMedCrossRef

Fantuzzi G. Adipose tissue, adipokines, and inflammation. J Allergy Clin Immunol. 2005;115(5):911–9. doi:10.1016/j.jaci.2005.02.023.PubMedCrossRef

Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 2004;89(6):2548–56. doi:10.1210/jc.2004-0395.PubMedCrossRef

Galic S, Oakhill JS, Steinberg GR. Adipose tissue as an endocrine organ. Mol Cell Endocrinol. 2010;316(2):129–39. doi:10.1016/j.mce.2009.08.018.PubMedCrossRef

Piya MK, McTernan PG, Kumar S. Adipokine inflammation and insulin resistance: the role of glucose, lipids and endotoxin. J Endocrinol. 2013;216(1):T1–T15. doi:10.1530/joe-12-0498.PubMedCrossRef

Matsubara M, Maruoka S, Katayose S. Inverse relationship between plasma adiponectin and leptin concentrations in normal-weight and obese women. Eur J Endocrinol. 2002;147(2):173–80. doi:10.1530/eje.0.1470173.PubMedCrossRef

Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402(6762):656–60. doi:10.1038/45230.PubMedCrossRef

Inui A, Asakawa A, Bowers CY, Mantovani G, Laviano A, Meguid MM, et al. Ghrelin, appetite, and gastric motility: the emerging role of the stomach as an endocrine organ. FASEB J Off Publ Fed Am Soc Exp Biol. 2004;18(3):439–56. doi:10.1096/fj.03-0641rev.

Williams DL, Cummings DE, Grill HJ, Kaplan JM. Meal-related ghrelin suppression requires postgastric feedback. Endocrinology. 2003;144(7):2765–7.PubMedCrossRef

10.

Fukushima N, Hanada R, Teranishi H, Fukue Y, Tachibana T, Ishikawa H, et al. Ghrelin directly regulates bone formation. J Bone Miner Res. 2005;20(5):790–8. doi:10.1359/JBMR.041237.PubMedCrossRef

11.

Sun Y, Ahmed S, Smith RG. Deletion of ghrelin impairs neither growth nor appetite. Mol Cell Biol. 2003;23(22):7973–81.PubMedCrossRef

12.

Sun Y, Wang P, Zheng H, Smith RG. Ghrelin stimulation of growth hormone release and appetite is mediated through the growth hormone secretagogue receptor. Proc Natl Acad Sci U S A. 2004;101(13):4679–84. doi:10.1073/pnas.0305930101.PubMedCrossRef

13.

Maccarinelli G, Sibilia V, Torsello A, Raimondo F, Pitto M, Giustina A, et al. Ghrelin regulates proliferation and differentiation of osteoblastic cells. J Endocrinol. 2005;184(1):249–56. doi:10.1677/joe.1.05837.PubMedCrossRef

14.

•• van der Velde M, van der Eerden BC, Sun Y, Almering JM, van der Lely AJ, Delhanty PJ, et al. An age-dependent interaction with leptin unmasks ghrelin's bone-protective effects. Endocrinology. 2012;153(8):3593–602. doi:10.1210/en.2012-1277. This paper examines the skeletal effects that each ghrelin and leptin has and is one of the first studies that explains the interplay that these 2 hormones have on bone in vivo.PubMedCrossRef

15.

Elefteriou F, Ahn JD, Takeda S, Starbuck M, Yang X, Liu X, et al. Leptin regulation of bone resorption by the sympathetic nervous system and CART. Nature. 2005;434(7032):514–20. http://www.nature.com/nature/journal/v434/n7032/suppinfo/nature03398_S1.html.PubMedCrossRef

16.

Guerardel A, Tanko LB, Boutin P, Christiansen C, Froguel P. Obesity susceptibility CART gene polymorphism contributes to bone remodeling in postmenopausal women. Osteoporos Int: a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. 2006;17(1):156–7. doi:10.1007/s00198-005-2022-1

17.

McLarnon A. Metabolism: age-dependent balance of leptin and ghrelin regulates bone metabolism. Nature Rev Endocrinol. 2012;8(9):504. doi:10.1038/nrendo.2012.116.CrossRef

18.

Nouh O, Abd Elfattah MM, Hassouna AA. Association between ghrelin levels and BMD: a cross sectional trial. Gynecol Endocrinol. 2012;28(7):570–2. doi:10.3109/09513590.2011.593663.PubMedCrossRef

19.

Wilasco MI, Goldani HA, Dornelles CT, Maurer RL, Kieling CO, Porowski M, et al. Ghrelin, leptin and insulin in healthy children: relationship with anthropometry, gender, and age distribution. Regul Pept. 2012;173(1–3):21–6. doi:10.1016/j.regpep.2011.08.013.PubMedCrossRef

20.

Napoli N, Pedone C, Pozzilli P, Lauretani F, Bandinelli S, Ferrucci L, et al. Effect of ghrelin on bone mass density: the InChianti study. Bone. 2011;49(2):257–63. doi:10.1016/j.bone.2011.03.772.PubMedCrossRef

21.

Pacifico L, Anania C, Poggiogalle E, Osborn JF, Prossomariti G, Martino F, et al. Relationships of acylated and des-acyl ghrelin levels to bone mineralization in obese children and adolescents. Bone. 2009;45(2):274–9. doi:10.1016/j.bone.2009.04.204.PubMedCrossRef

22.

Cigdem Arica P, Kocael A, Tabak O, Taskin M, Zengin K, Uzun H. Plasma ghrelin, leptin, and orexin-A levels and insulin resistance after laparoscopic gastric band applications in morbidly obese patients. Minerva Medica. 2013;104(3):309–16.PubMed

23.

•• Brzozowska MM, Sainsbury A, Eisman JA, Baldock PA, Center JR. Bariatric surgery, bone loss, obesity and possible mechanisms. Obes Rev. 2013;14(1):52–67. doi:10.1111/j.1467-789X.2012.01050.x. This review assesses the interactions between bariatric surgery, bone loss, and obesity. Obesity and bone loss has been widely overlooked; evidence suggests that continued bone loss is present in postbariatric surgery. This review extensively examines the current literature and suggests possible mechanisms that may be occurring.PubMedCrossRef

24.

Shapses SA, Riedt CS. Bone, body weight, and weight reduction: what are the concerns? J Nutrition. 2006;136(6):1453–6.

25.

Wong IP, Baldock PA, Herzog H. Gastrointestinal peptides and bone health. Curr Opin Endocrinol Diabetes Obes. 2010;17(1):44–50. doi:10.1097/MED.0b013e3283344a05.PubMed

26.

Walsh JS, Henriksen DB. Feeding and bone. Arch Biochemis Biophys. 2010;503(1):11–9. doi:10.1016/j.abb.2010.06.020.CrossRef

27.

•• Wong IPL, Driessler F, Khor EC, Shi Y-C, Hörmer B, Nguyen AD, et al. Peptide YY regulates bone remodeling in mice: a link between gut and skeletal biology. PLoS One. 2012;7(7):e40038. doi:10.1371/journal.pone.0040038. This study showed that PYY regulates bone remodelling via the osteoblastic Y1 receptor using knockout and transgenic mice.PubMedCrossRef

28.

Wortley KE, Garcia K, Okamoto H, Thabet K, Anderson KD, Shen V, et al. Peptide YY regulates bone turnover in rodents. Gastroenterology. 2007;133(5):1534–43. doi:10.1053/j.gastro.2007.08.024.PubMedCrossRef

29.

Yuzuriha H, Inui A, Asakawa A, Ueno N, Kasuga M, Meguid MM, et al. Gastrointestinal hormones (anorexigenic peptide YY and orexigenic ghrelin) influence neural tube development. FASEB J. 2007;21(9):2108–12. doi:10.1096/fj.06-7621com.PubMedCrossRef

30.

Angelopoulos N, Goula A, Tolis G. Current knowledge in the neurophysiologic modulation of obesity. Metab Clin Exp. 2005;54(9):1202–17. doi:10.1016/j.metabol.2005.04.005.PubMedCrossRef

31.

Misra M, Miller KK, Tsai P, Gallagher K, Lin A, Lee N, et al. Elevated peptide YY levels in adolescent girls with anorexia nervosa. J Clin Endocrinol Metabol. 2006;91(3):1027–33. doi:10.1210/jc.2005-1878.CrossRef

32.

Howgate DJ, Graham SM, Leonidou A, Korres N, Tsiridis E, Tsapakis E. Bone metabolism in anorexia nervosa: molecular pathways and current treatment modalities. Osteoporo Int. 2013;24(2):407–21. doi:10.1007/s00198-012-2095-6.CrossRef

33.

Scheid JL, Toombs RJ, Ducher G, Gibbs JC, Williams NI, De Souza MJ. Estrogen and peptide YY are associated with bone mineral density in premenopausal exercising women. Bone. 2011;49(2):194–201. doi:10.1016/j.bone.2011.04.011.PubMedCrossRef

34.

Batterham RL, Cohen MA, Ellis SM, Le Roux CW, Withers DJ, Frost GS, et al. Inhibition of food intake in obese subjects by Peptide YY3–36. N Engl J Med. 2003;349(10):941–8. doi:10.1056/NEJMoa030204.PubMedCrossRef

35.

Reid IR. Relationships among body mass, its components, and bone. Bone. 2002;31(5):547–55.PubMedCrossRef

36.

Utz AL, Lawson EA, Misra M, Mickley D, Gleysteen S, Herzog DB, et al. Peptide YY (PYY) levels and bone mineral density (BMD) in women with anorexia nervosa. Bone. 2008;43(1):135–9. doi:10.1016/j.bone.2008.03.007.PubMedCrossRef

37.

Misra M, Prabhakaran R, Miller KK, Goldstein MA, Mickley D, Clauss L, et al. Prognostic indicators of changes in bone density measures in adolescent girls with anorexia nervosa-II. J Clin Endocrinol Metabol. 2008;93(4):1292–7. doi:10.1210/jc.2007-2419.CrossRef

38.

Clowes JA, Khosla S, Eastell R. Potential role of pancreatic and enteric hormones in regulating bone turnover. J Bone Min Res. 2005;20(9):1497–506. doi:10.1359/JBMR.050524.CrossRef

39.

Asmar M, Holst JJ. Glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide: new advances. Curr Opin Endocrinol Diabetes Obes. 2010;17(1):57–62. doi:10.1097/MED.0b013e3283339051.PubMed

40.

Paschetta E, Hvalryg M, Musso G. Glucose-dependent insulinotropic polypeptide: from pathophysiology to therapeutic opportunities in obesity-associated disorders. Obes Rev. 2011;12(10):813–28. doi:10.1111/j.1467-789X.2011.00897.x.PubMedCrossRef

41.

Tsukiyama K, Yamada Y, Yamada C, Harada N, Kawasaki Y, Ogura M, et al. Gastric inhibitory polypeptide as an endogenous factor promoting new bone formation after food ingestion. Mol Endocrinol. 2006;20(7):1644–51. doi:10.1210/me.2005-0187.PubMedCrossRef

42.

Xie D, Zhong Q, Ding KH, Cheng H, Williams S, Correa D, et al. Glucose-dependent insulinotropic peptide-overexpressing transgenic mice have increased bone mass. Bone. 2007;40(5):1352–60. doi:10.1016/j.bone.2007.01.007.PubMedCrossRef

43.

Xie D, Cheng H, Hamrick M, Zhong Q, Ding K-H, Correa D, et al. Glucose-dependent insulinotropic polypeptide receptor knockout mice have altered bone turnover. Bone. 2005;37(6):759–69. doi:10.1016/j.bone.2005.06.021.PubMedCrossRef

44.

Gaudin-Audrain C, Irwin N, Mansur S, Flatt PR, Thorens B, Basle M, et al. Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice. Bone. 2013;53(1):221–30. doi:10.1016/j.bone.2012.11.039.PubMedCrossRef

45.

Nuche-Berenguer B, Moreno P, Esbrit P, Dapia S, Caeiro JR, Cancelas J, et al. Effect of GLP-1 treatment on bone turnover in normal, type 2 diabetic, and insulin-resistant states. Calcif Tissue Int. 2009;84(6):453–61. doi:10.1007/s00223-009-9220-3.PubMedCrossRef

46.

• Pacheco-Pantoja EL, Ranganath LR, Gallagher JA, Wilson PJ, Fraser WD. Receptors and effects of gut hormones in three osteoblastic cell lines. BMC Physiol. 2011;11:12. doi:10.1186/1472-6793-11-12. This paper outlines the response of cell lines to GLP-2 and explains that osteoblastic maturation may be a factor in explaining the different responses observed.PubMedCrossRef

47.

Henriksen DB, Alexandersen P, Bjarnason NH, Vilsboll T, Hartmann B, Henriksen EE, et al. Role of gastrointestinal hormones in postprandial reduction of bone resorption. J Bone Miner Res. 2003;18(12):2180–9. doi:10.1359/jbmr.2003.18.12.2180.PubMedCrossRef

48.

Henriksen DB, Alexandersen P, Byrjalsen I, Hartmann B, Bone HG, Christiansen C, et al. Reduction of nocturnal rise in bone resorption by subcutaneous GLP-2. Bone. 2004;34(1):140–7.PubMedCrossRef

49.

Henriksen DB, Alexandersen P, Hartmann B, Adrian CL, Byrjalsen I, Bone HG, et al. Disassociation of bone resorption and formation by GLP-2: a 14-day study in healthy postmenopausal women. Bone. 2007;40(3):723–9. doi:10.1016/j.bone.2006.09.025.PubMedCrossRef

50.

Henriksen DB, Alexandersen P, Hartmann B, Adrian CL, Byrjalsen I, Bone HG, et al. Four-month treatment with GLP-2 significantly increases hip BMD: a randomized, placebo-controlled, dose-ranging study in postmenopausal women with low BMD. Bone. 2009;45(5):833–42. doi:10.1016/j.bone.2009.07.008.PubMedCrossRef

51.

Dicembrini I, Mannucci E, Rotella CM. Bone: incretin hormones perceiver or receiver? Exp Diabetes Res. 2012;2012:519784. doi:10.1155/2012/519784.PubMedCrossRef

52.

Askov-Hansen C, Jeppesen PB, Lund P, Hartmann B, Holst JJ, Henriksen DB. Effect of glucagon-like peptide-2 exposure on bone resorption: effectiveness of high concentration versus prolonged exposure. Regul Pept. 2012;181C:4–8. doi:10.1016/j.regpep.2012.11.002.

53.

Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292–5. doi:10.1056/NEJM199602013340503.PubMedCrossRef

54.

Chen H, Charlat O, Tartaglia LA, Woolf EA, Weng X, Ellis SJ, et al. Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db/db Mice. Cell. 1996;84(3):491–5. doi:10.1016/S0092-8674(00)81294-5.PubMedCrossRef

55.

Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372(6505):425–32.PubMedCrossRef

56.

Baldock PA, Sainsbury A, Allison S, Lin EJ, Couzens M, Boey D, et al. Hypothalamic control of bone formation: distinct actions of leptin and y2 receptor pathways. J Bone Miner Res. 2005;20(10):1851–7. doi:10.1359/JBMR.050523.PubMedCrossRef

57.

Baldock PA, Allison S, McDonald MM, Sainsbury A, Enriquez RF, Little DG, et al. Hypothalamic regulation of cortical bone mass: opposing activity of Y2 receptor and leptin pathways. J Bone Miner Res. 2006;21(10):1600–7. doi:10.1359/jbmr.060705.PubMedCrossRef

58.

Hamrick MW, Pennington C, Newton D, Xie D, Isales C. Leptin deficiency produces contrasting phenotypes in bones of the limb and spine. Bone. 2004;34(3):376–83. doi:10.1016/j.bone.2003.11.020.PubMedCrossRef

59.

Lee NJ, Wong IP, Baldock PA, Herzog H. Leptin as an endocrine signal in bone. Curr Osteoporos Rep. 2008;6(2):62–6.PubMedCrossRef

60.

Vaisse C, Halaas JL, Horvath CM, Darnell Jr JE, Stoffel M, Friedman JM. Leptin activation of Stat3 in the hypothalamus of wild-type and ob/ob mice but not db/db mice. Nat Genet. 1996;14(1):95–7. doi:10.1038/ng0996-95.PubMedCrossRef

61.

Ducy P, Amling M, Takeda S, Priemel M, Schilling AF, Beil FT, et al. Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass. Cell. 2000;100(2):197–207. doi:10.1016/S0092-8674(00)81558-5.PubMedCrossRef

62.

Iwaniec UT, Boghossian S, Lapke PD, Turner RT, Kalra SP. Central leptin gene therapy corrects skeletal abnormalities in leptin-deficient ob/ob mice. Peptides. 2007;28(5):1012–9. doi:10.1016/j.peptides.2007.02.001.PubMedCrossRef

63.

Takeda S, Elefteriou F, Levasseur R, Liu X, Zhao L, Parker KL, et al. Leptin regulates bone formation via the sympathetic nervous system. Cell. 2002;111(3):305–17. doi:10.1016/S0092-8674(02)01049-8.PubMedCrossRef

64.

Kajimura D, Hinoi E, Ferron M, Kode A, Riley KJ, Zhou B, et al. Genetic determination of the cellular basis of the sympathetic regulation of bone mass accrual. J Exp Med. 2011;208(4):841–51. doi:10.1084/jem.20102608.PubMedCrossRef

65.

Wilding JP, Gilbey SG, Bailey CJ, Batt RA, Williams G, Ghatei MA, et al. Increased neuropeptide-Y messenger ribonucleic acid (mRNA) and decreased neurotensin mRNA in the hypothalamus of the obese (ob/ob) mouse. Endocrinology. 1993;132(5):1939–44. doi:10.1210/en.132.5.1939.PubMedCrossRef

66.

Stephens TW, Basinski M, Bristow PK, Bue-Valleskey JM, Burgett SG, Craft L, et al. The role of neuropeptide Y in the antiobesity action of the obese gene product. Nature. 1995;377(6549):530–2.PubMedCrossRef

67.

Baldock PA, Allison SJ, Lundberg P, Lee NJ, Slack K, Lin E-JD, et al. Novel role of Y1 receptors in the coordinated regulation of bone and energy homeostasis. J Biolog Chemis. 2007;282(26):19092–102. doi:10.1074/jbc.M700644200.CrossRef

68.

Baldock PA, Lee NJ, Driessler F, Lin S, Allison S, Stehrer B, et al. Neuropeptide Y knockout mice reveal a central role of NPY in the coordination of bone mass to body weight. PLoS One. 2009;4(12):e8415. doi:10.1371/journal.pone.0008415.PubMedCrossRef

69.

Baldock PA, Sainsbury A, Couzens M, Enriquez RF, Thomas GP, Gardiner EM, et al. Hypothalamic Y2 receptors regulate bone formation. J Clin Invest. 2002;109(7):915–21. doi:10.1172/JCI14588.PubMed

70.

•• Wong IPL, Nguyen AD, Khor EC, Enriquez RF, Eisman JA, Sainsbury A, et al. Neuropeptide Y is a critical modulator of Leptin's regulation of cortical bone. J Bone Miner Res. 2013;28(4):886–98. doi:10.1002/jbmr.1786. This study showed the contribution of NPY in the cortical bone phenotype of ob/ob mice.PubMedCrossRef

71.

Cornish J, Callon KE, Bava U, Lin C, Naot D, Hill BL, et al. Leptin directly regulates bone cell function in vitro and reduces bone fragility in vivo. J Endocrinol. 2002;175(2):405–15.PubMedCrossRef

72.

Lee YJ, Park JH, Ju SK, You KH, Ko JS, Kim HM. Leptin receptor isoform expression in rat osteoblasts and their functional analysis. FEBS Lett. 2002;528(1–3):43–7.PubMedCrossRef

73.

Steppan CM, Crawford DT, Chidsey-Frink KL, Ke H, Swick AG. Leptin is a potent stimulator of bone growth in ob/ob mice. Regul Pept. 2000;92(1–3):73–8. doi:10.1016/S0167-0115(00)00152-X.PubMedCrossRef

74.

Nakajima R, Inada H, Koike T, Yamano T. Effects of leptin to cultured growth plate chondrocytes. Horm Res. 2003;60(2):91–8.PubMedCrossRef

75.

Reseland JE, Syversen U, Bakke I, Qvigstad G, Eide LG, Hjertner O, et al. Leptin is expressed in and secreted from primary cultures of human osteoblasts and promotes bone mineralization. J Bone Miner Res. 2001;16(8):1426–33. doi:10.1359/jbmr.2001.16.8.1426.PubMedCrossRef

76.

Burguera B, Hofbauer LC, Thomas T, Gori F, Evans GL, Khosla S, et al. Leptin reduces ovariectomy-induced bone loss in rats. Endocrinology. 2001;142(8):3546–53. doi:10.1210/en.142.8.3546.PubMedCrossRef

77.

Jackson MA, Iwaniec UT, Turner RT, Wronski TJ, Kalra SP. Effects of increased hypothalamic leptin gene expression on ovariectomy-induced bone loss in rats. Peptides. 2011;32(8):1575–80. doi:10.1016/j.peptides.2011.04.029.PubMedCrossRef

78.

•• Turner RT, Kalra SP, Wong CP, Philbrick KA, Lindenmaier LB, Boghossian S, et al. Peripheral leptin regulates bone formation. J Bone Miner Res. 2013;28(1):22–34. doi:10.1002/jbmr.1734. The role of peripheral leptin signalling in bone remodelling was revisited in this study.PubMedCrossRef

79.

Williams LM. Hypothalamic dysfunction in obesity. Proc Nutr Soc. 2012;71(4):521–33. doi:10.1017/S002966511200078X.PubMedCrossRef

80.

Hamrick MW, Ding KH, Ponnala S, Ferrari SL, Isales CM. Caloric restriction decreases cortical bone mass but spares trabecular bone in the mouse skeleton: implications for the regulation of bone mass by body weight. J Bone Miner Res. 2008;23(6):870–8. doi:10.1359/jbmr.080213.PubMedCrossRef

81.

Farooqi IS, Jebb SA, Langmack G, Lawrence E, Cheetham CH, Prentice AM, et al. Effects of recombinant leptin therapy in a child with congenital leptin deficiency. N Engl J Med. 1999;341(12):879–84. doi:10.1056/NEJM199909163411204.PubMedCrossRef

82.

Ahmadi F, Salari S, Maziar S, Esfahanian F, Khazaeipour Z, Ranjbarnovin N. Relationship between serum leptin levels and bone mineral density and bone metabolic markers in patients on hemodialysis. Saudi J Kidney Dis Transpl. 2013;24(1):41–7.

83.

Zhao H-Z, Bi Y-F, Ma L-Y, Zhao L, Wang T-G, Zhang L-Z, et al. The effects of bisphenol A (BPA) exposure on fat mass and serum leptin concentrations have no impact on bone mineral densities in nonobese premenopausal women. Clin Biochemis. 2012;45(18):1602–6. doi:10.1016/j.clinbiochem.2012.08.024.CrossRef

84.

Thomas T, Burguera B, Melton III LJ, Atkinson EJ, O'Fallon WM, Riggs BL, et al. Role of serum leptin, insulin, and estrogen levels as potential mediators of the relationship between fat mass and bone mineral density in men versus women. Bone. 2001;29(2):114–20.PubMedCrossRef

85.

Sienkiewicz E, Magkos F, Aronis KN, Brinkoetter M, Chamberland JP, Chou S, et al. Long-term metreleptin treatment increases bone mineral density and content at the lumbar spine of lean hypoleptinemic women. Metab Clin Exp. 2011;60(9):1211–21. doi:10.1016/j.metabol.2011.05.016.PubMedCrossRef

86.

Conroy R, Girotra M, Shane E, McMahon DJ, Pavlovich KH, Leibel RL, et al. Leptin administration does not prevent the bone mineral metabolism changes induced by weight loss. Metab Clin Exp. 2011;60(9):1222–6. doi:10.1016/j.metabol.2011.02.010.PubMedCrossRef

87.

Hu E, Liang P, Spiegelman BM. AdipoQ is a novel adipose-specific gene dysregulated in obesity. J Biologic Chemis. 1996;271(18):10697–703.CrossRef

88.

Berner HS, Lyngstadaas SP, Spahr A, Monjo M, Thommesen L, Drevon CA, et al. Adiponectin and its receptors are expressed in bone-forming cells. Bone. 2004;35(4):842–9. doi:10.1016/j.bone.2004.06.008.PubMedCrossRef

89.

Luo X-H, Guo L-J, Yuan L-Q, Xie H, Zhou H-D, Wu X-P, et al. Adiponectin stimulates human osteoblasts proliferation and differentiation via the MAPK signaling pathway. Exp Cell Res. 2005;309(1):99–109. doi:10.1016/j.yexcr.2005.05.021.PubMedCrossRef

90.

Shinoda Y, Yamaguchi M, Ogata N, Akune T, Kubota N, Yamauchi T, et al. Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways. J Cell Biochemis. 2006;99(1):196–208. doi:10.1002/jcb.20890.CrossRef

91.

Zhang Y, Zhou P, Kimondo JW. Adiponectin and osteocalcin: relation to insulin sensitivity. Biochem Cell Biol. 2012;90(5):613–20. doi:10.1139/o2012-022.PubMedCrossRef

Title: Influence of Hormonal Appetite and Energy Regulators on Bone
Authors: Ee Cheng Khor
Natalie Kah Yun Wee
Paul A Baldock
Publication date: 01-09-2013
Publisher: Springer US
Published in: Current Osteoporosis Reports / Issue 3/2013
Print ISSN: 1544-1873
Electronic ISSN: 1544-2241
DOI: https://doi.org/10.1007/s11914-013-0157-0

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Influence of Hormonal Appetite and Energy Regulators on Bone

Abstract

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Abstract

Please log in to get access to this content

Other articles of this Issue 3/2013

Impact of the Environment on the Skeleton: Is it Modulated by Genetic Factors?

Vitamin B12, Folic Acid, and Bone

The Women’s Health Initiative: Hormone Therapy and Calcium/Vitamin D Supplementation Trials

Atypical Femoral fractures: A Review of the Literature

Computational Anatomy in the Study of Bone Structure

Vitamin D and Skeletal Growth and Development